|Application ||WB, IHC-P, FC, E|
|Calculated MW||52913 Da|
|Antigen Region||116-144 aa|
|Other Names||Wiskott-Aldrich syndrome protein, WASp, WAS, IMD2|
|Target/Specificity||This WAS antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 116-144 amino acids from the Central region of human WAS.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||WAS Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Effector protein for Rho-type GTPases. Regulates actin filament reorganization via its interaction with the Arp2/3 complex. Important for efficient actin polymerization. Possible regulator of lymphocyte and platelet function. Mediates actin filament reorganization and the formation of actin pedestals upon infection by pathogenic bacteria.|
|Cellular Location||Cytoplasm, cytoskeleton.|
|Tissue Location||Expressed predominantly in the thymus. Also found, to a much lesser extent, in the spleen|
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Provided below are standard protocols that you may find useful for product applications.
The Wiskott-Aldrich syndrome (WAS) family of proteins share similar domain structure, and are involved in transduction of signals from receptors on the cell surface to the actin cytoskeleton. The presence of a number of different motifs suggests that they are regulated by a number of different stimuli, and interact with multiple proteins. Recent studies have demonstrated that these proteins, directly or indirectly, associate with the small GTPase, Cdc42, known to regulate formation of actin filaments, and the cytoskeletal organizing complex, Arp2/3. Wiskott-Aldrich syndrome is a rare, inherited, X-linked, recessive disease characterized by immune dysregulation and microthrombocytopenia, and is caused by mutations in the WAS gene. The WAS gene product is a cytoplasmic protein, expressed exclusively in hematopoietic cells, which show signalling and cytoskeletal abnormalities in WAS patients.
Rajmohan, R., et al. FEMS Yeast Res. 9(8):1226-1235(2009)
Dovas, A., et al. J. Cell. Sci. 122 (PT 21), 3873-3882 (2009)
Cammer, M., et al. J. Biol. Chem. 284(35):23302-23311(2009)
Zhang, J., et al. J. Biol. Chem. 284(32):21659-21669(2009)
Ameratunga, R., et al. N. Z. Med. J. 122(1304):46-53(2009)
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